• Da Zhang.
• Department of Emergency Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
• Am J Emerg Med. 2012 Nov 1;30(9):2039-45.

BackgroundPostresuscitation myocardial dysfunction contributes to the low survival rate after successful resuscitation, but its mechanism remains poorly understood. This study investigated whether caspase 3-mediated apoptosis is activated in the heart after postresuscitation myocardial dysfunction.MethodsAfter pigs were subjected to 8 minutes of electrically induced cardiac arrest (CA), standard cardiopulmonary resuscitation was performed. Animals in the post-return of spontaneous circulation (ROSC) group were randomly assigned to be killed (n = 6 per group) at 12 and 24 hours after ROSC, and myocardial specimens were analyzed with electron microscopy, Western blotting, quantitative real-time polymerase chain reaction, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay.ResultsMyocardial function was significantly impaired after ROSC. Expression of Bcl-2, Bax, and caspase 3 protein was markedly increased in the post-ROSC group compared with the sham-operated group (P < .05) at 12 and 24 hours after ROSC, whereas Bcl-2/Bax was significantly reduced in the post-ROSC group compared with the sham-operated group (P < .05). The messenger RNA levels of caspase 3 were significantly elevated at 12 and 24 hours after ROSC, and increases in caspase 3 activity indicated activation of the mitochondrial apoptotic pathway. Typical apoptotic nuclei were observed in cardiomyocytes 24 hours after ROSC. More apoptotic cells were observed in animals that had undergone CA compared with sham-operated animals (P < .05).ConclusionCaspase 3-mediated apoptosis may be one of the main pathologic mechanisms of postresuscitation myocardial injury in a porcine model of CA.Copyright © 2012 Elsevier Inc. All rights reserved.

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